Crossbridge phosphorylation and regulation of vascular smooth muscle contraction

A model is proposed to explain crossbridge regulation in smooth muscle and the latch state (high force with very low crossbridge cycling rates). The model predicts that low levels of [Ca2+] and myosin phosphorylation can induce high values of force. In this analysis we show that reductions in myosin light chain phosphatase activity make stress more proportional to phosphorylation, with abolition of the latch state. This may explain some of the differences in the phosphorylation dependence of force between intact and skinned smooth muscle.